Melanoma location and its significance for prognosis Lachiewicz AM, Berwick M, Wiggins CL, Thomas NE Arch Dermatol 2008: 114(4): 515-21 Melanoma cases continue to increase and methods of predicting prognosis and alerting the population to appropriate and accurate screening remain important in managing this problem.

The American Joint Committee on Cancer has identified Breslow thickness, ulceration, nodal and distant metastases and several other factors as critical staging criteria, but the significance of melanoma site in prognosis is still debated.

This cohort study performed in the US was designed to compare prognosis in those with melanoma sited on the scalp or neck with that of patients with melanomas at other sites. It was a large study of 51,704 white, non-Hispanic adults. The study was performed retrospectively using the National Cancer Institute SEER Program and collected data on patients diagnosed with their first invasive melanoma.

The researchers found 6 per cent of the melanomas were located on the scalp or neck and these patients were older, presented with thicker tumours and were more likely to be male. The tumours were also more likely to be ulcerated and to have positive lymph nodes. They had a 1.84 times higher rate of death even after controlling for age, Breslow thickness, sex and ulceration. The five- and 10-year survival probabilities were lower in the scalp and neck melanomas compared with other sites and although accounting for just 6 per cent of cases, they were responsible for 10 per cent of all deaths from melanoma.

The authors concluded from these data that there is a notable survival difference between scalp and neck melanoma and melanoma at other sites, even after adjusting for important prognostic factors. The reason for the worse survival rate is unclear, but they speculated that the lymphatic drainage is complex and these tumours have a markedly higher incidence of brain metastases and may not receive adequate margin resection owing to cosmetic or functional concerns. These tumours are often hidden by the hairline and may have a poorer prognosis as a result of late diagnosis.

Despite flaws in this study, such as the limited population, some susceptibility to selection bias and missing data in the SEER database leading to some cases having to be excluded, this does appear quite a robust piece of research, with some promising evidence for another potential prognostic factor.

In terms of day-to-day practice, it should alert us to the importance of checking the scalp and neck, improving education for patients in terms of screening and alerting them to these sites, and, as the authors suggest, perhaps targeting education to hairdressers about melanomas of the scalp and neck. We might even start receiving referrals from salons.Dr Jane Barnard is a GP with an interest in dermatology in Yateley, Hampshire

Gender differences and the effect of the atopic march Lowe AJ, Carlin JB, Catherine M et al. J Allergy Clin Immunol 2008; 121(5): 1190-5 The atopic march is the hypothesis that infants with eczema are at increased risk of developing childhood asthma. Recent research argues that eczema is not a risk factor unless there is also sensitisation or early wheezing.

This study looked at the role of infantile eczema as a predictor of childhood asthma, while allowing for the effects of early wheeze, sensitisation and sex, both as independent effects and possible effect modifiers.

This prospective study of 620 infants with a significant family history of atopy involved a telephone survey every four weeks from birth to the age of 64 weeks, then at 78 weeks, two years and annually thereafter until seven years of age. Sensitisation was determined with skin prick tests at six, 12 and 24 months to six common food and inhalant allergens.

The results showed that almost half developed eczema in the first two years of life and this doubled the odds of childhood asthma at age six and seven years. This appeared greatest for eczema presenting in the first six months of life, male sex and the presence of sensitisation and wheezing within the first two years of life.

Eczema was associated with a greater increase in risk of childhood asthma in boys (OR 3.05) than in girls (OR 1.44), with the difference remaining statistically significant in boys when adjustments for early wheeze and sensitisation were made. With adjustment for sensitisation alone, it demonstrated a reduction in the risk, suggesting that in boys, some of the association between early eczema and risk of asthma is mediated by an increase in sensitisation.

There were a number of limitations to the study, including the use of telephone surveys with parents for the follow-ups, 217 children lost to follow-up, weak diagnosis of eczema and asthma, and sensitisation tests for six allergens only. The study does, however, raise some interesting points if its findings are accurate. First, boys are much more susceptible to the atopic march than girls, and understanding why these differences occur may provide opportunities for new interventions to prevent the development of asthma. Second, the suggestion that sensitisation could be a mediating factor in the development of childhood asthma. There is a growing body of evidence that sensitisation can occur through damaged skin and if the increased risk of asthma is in part mediated by the development of allergic sensitisation, then theoretically, by improving the barrier function in infants with eczema who are yet to develop sensitisation, we might reduce their risk of developing asthma. Clearly, further research with more robust data collection is needed, but we watch this space with anticipation. JB

Evidence about the effect of biological detergents on skin Basketter DA, English JSC, Wakelin SH, White IR. Br J Dermatol 2008; 158(6): 1177-81 People have been laundering clothes for millennia. However, the use of soaps and detergents is relatively new, having been introduced in the late 19th century. Proteolytic enzymes first appeared in laundry products in the mid-20th century.

The introduction of these enzymes allowed for the removal of dirt and stains at lower temperatures. More recently, other enzyme classes, such as amylases and lipases, have been added, further increasing the power of these detergents.

For many years in the UK, patients and healthcare professionals have believed that these enzymes can lead to adverse skin reactions. Many patients with skin disease have been advised to change their detergent to non-biological products, in the hope that this might resolve their problem. The authors of this review paper examined the literature to see if there was any foundation to this belief.

It has long been recognised that occupational exposure in the manufacture of biological detergents can lead to respiratory allergy and skin irritation. However, strict exposure control for workers in this industry has largely solved these problems.

Early studies did show an increased risk of irritant reactions with exaggerated product use, for example, direct patch testing with raw product. However, review of the literature has shown conclusively that in actual consumer use, the enzymes in detergents do not lead to an increased risk of either irritant or allergic reactions. Investigations of many patients with skin disease thought to be due to laundry products have shown that enzymes were not responsible.

In theory, enzymes are capable of triggering the formation of IgE antibodies, as with other proteins (for example, natural rubber latex proteins), which could lead to an immediate type I hypersensitivity reaction. However, in practice, there is no evidence for this in either occupational or consumer use.

The authors concluded that enzymes incorporated in detergents have an extensive history of safe use in the consumer market. They also have a beneficial environmental effect, owing to their biodegradability and functionality at low temperatures. The perceived harmful effect on skin seems to be based on mythology. Therefore, skin complaints should not be dismissed as a result of enzyme-containing detergents and patients should be investigated for the true cause of the problem.Dr Waseem Chaudhry is a GPSI in dermatology in Caerphilly

Clinically, it presents as erythema three to five hours after exposure, reaching a maximum at 12 to 24 hours and gradually fading after 48 hours. Symptoms can range from mild redness to painful erythema, blistering and induration. Severe cases can exhibit systemic symptoms, such as fever, chills and dehydration. Current therapy for sunburn is to use topical corticosteroids for symptomatic relief. This is controversial and has a poor evidence base.

This study examined the effectiveness of moderate and potent topical corticosteroids in the treatment of sunburn. Twenty healthy volunteers with skin type I (always burns, rarely tans) were selected.

Each volunteer had seven 32cm2 areas marked on the upper back. One untreated area was used to determine UV sensitivity. Two areas were treated with moderate or potent topical steroid 30 minutes before UVB exposure (controls). Two areas were treated with moderate or potent topical steroid six hours after UVB exposure and the remaining two areas were treated with moderate or potent topical steroid 23 hours after UVB exposure.

The minimal erythema dose (MED) was defined as the amount of UVB needed to produce just perceptible erythema. The main outcome measure was defined as the sunburn improvement factor (SIF) using the equation: SIF = MED on treated skin/MED on non-treated skin. Therefore, a SIF >1 indicated a beneficial effect of topical corticosteroids in the relief of sunburn.

Results showed that SIFs in areas treated with either topical corticosteroid 30 minutes before UVB exposure or potent topical corticosteroid six hours after UVB exposure were significantly higher than SIFs in non-treated areas.

The only clinically relevant improvement was seen in the areas treated with potent topical corticosteroids 30 minutes before UVB exposure. The authors postulated that this was due to the vasoconstrictive effect of the topical corticosteroid, which would lead to a reduction in the release of inflammatory mediators at the time of the UVB exposure.

The areas treated 23 hours after UVB exposure and areas treated with a moderate potency topical corticosteroid showed no significant reduction in erythema. Therefore, treatment with moderate or potent topical corticosteroids at either six or 23 hours after exposure does not lead to a reduction in acute sunburn reaction. However, pre-treatment with potent topical corticosteroid does have a clinical benefit.

The authors felt that patients using potent topical corticosteroids, for example, those with eczema, are not at a higher risk of sunburn and may possibly have some sun protection from their treatment. WC.

Register or Subscribe to MIMS

GPs can get MIMS print & online and GPonline for free when they register online – take 2 minutes, and make sure you get your free MIMS access! If you're not a GP, you can subscribe to MIMS for full access.